Rates of Seed Treatment Insecticides and Control of Stewart's Wilt in Sweet Corn.

Neonicotinoid insecticides applied as seed treatments reduce the incidence of Stewart's wilt. The objectives of this study were to examine the efficacy of different rates of seed treatment insecticides to control Stewart's wilt on susceptible sweet corn hybrids and to compare the economic value of Stewart's wilt control in sweet corn grown for processing and fresh market. Clothianidin (Poncho), imidacloprid (Gaucho), and thiamethoxam (Cruiser) applied to seed at rates ranging from 0.125 to 1.25 mg a.i. per kernel were evaluated in 11 field trials in Illinois and Delaware from 2000 to 2003. Incidence of Stewart's wilt was significantly lower when seed was treated with insecticides than when plants were grown from nontreated seed in all but one trial. The level of control usually was between 50 and 90%. Small but statistically significant differences in incidence of systemically infected plants occurred among rates of insecticides in all trials except those in 2001. Usually, incidence of systemic Stewart's wilt was lower when higher rates of insecticides were applied; however, increasing the rate of insecticides from 0.125 mg a.i. to 1.25 mg a.i. per kernel had a relatively small effect on the level of Stewart's wilt control compared with the difference between treated and nontreated sweet corn seed. Based on a regression analysis, the lowest rates of the insecticides provided 64 to 72% control. The level of control increased about 1.85% with each additional 0.1 mg a.i. of insecticide per kernel from 0.125 mg a.i. to 1.25 mg a.i. Clothianidin provided an 8 or 9% higher level of control than thiamethoxam or imidacloprid at the same rate. Recommendations for application of seed treatment insecticides to processing and fresh market sweet corn differed somewhat due to substantial differences in the value of the crops. Based on estimated costs of $6 to $12 per 0.4 ha for the seed treatments, the economic break even point (i.e., cost of control = value from control) occurred in the range of 3 to 6% Stewart's wilt incidence for processing sweet corn valued at $325 per 0.4 ha and at about 1% Stewart's wilt incidence for fresh market sweet corn valued at $1,625 per 0.4 ha. Relatively small differences in levels of control conferred by commercially available rates of clothianidin (0.25 mg a.i. per kernel) and thiamethoxam (0.125 mg a.i. per kernel) were of little consequence in processing sweet corn but had considerable economic value in fresh market sweet corn.

Control of Stewart's Wilt in Sweet Corn with Seed Treatment Insecticides.

Corn flea beetles, Chaetocnema pulicaria, vector Erwinia stewartii (synamorph Pantoea stewartii), which causes Stewart's bacterial wilt of corn (Zea mays). A seed treatment insecticide, imidacloprid, killed flea beetles and reduced the number of feeding wounds and Stewart's wilt symptoms per leaf in greenhouse studies. The objective of our research was to evaluate the ability of imidacloprid and thiamethoxam seed treatments to control Stewart's wilt on sweet corn hybrids under field conditions with naturally occurring populations of the corn flea beetle. Six field trials were planted at four locations in 1998. Eleven field trials were planted at nine locations in 1999. The treatment design was a factorial of sweet corn hybrids and seed treatments. Stewart's wilt incidence ranged from 0 to 54% in the 1998 trials. Incidence of Stewart's wilt in nontreated plots of the susceptible hybrid Jubilee ranged from 2% at the 8-leaf stage to 77% 1 week after mid-silk in the 1999 trials. Seed treatment insecticides reduced the incidence of Stewart's wilt by ≈50 to 85% relative to nontreated controls. The level of control was ≈75 to 85% in seven trials planted before 1 June 1999, when incidence of Stewart's wilt on nontreated Jubilee ranged from 4 to 71%. The level of control was ≈50 to 70% in the three trials planted after 1 July 1999, when incidence of Stewart's wilt on nontreated Jubilee ranged from 44 to 73%. Although comparisons varied, the level of control gained from seed treatment insecticides was similar to the next higher level of host resistance. Seed treatment insecticides appear to control Stewart's wilt during very early growth of corn plants, when foliar applications of insecticides are ineffective and the effectiveness of host resistance varies depending on the proximity of flea beetle feeding sites to the plant's growing point.

First Report of Puccinia sorghi Virulent on Sweet Corn with the Rp1-D Gene in Florida and Texas.

For the past 15 years, the Rp1-D gene has controlled common rust on sweet corn in North America. In August and September 1999, isolates of Puccinia sorghi were collected from Rp1-D sweet corn hybrids in Illinois, Wisconsin, Minnesota, Michigan, and New York. This was the first widespread occurrence in the continental United States of P. sorghi virulent on the Rp1-D gene (1). Isolates of P. sorghi collected from Los Mochis, Mexico, in March 2000 had a pattern of virulence similar to the pattern for the isolates collected in the Midwest in 1999 (2). In April and May 2000, small uredinia were observed on Rp1-D sweet corn in Florida and Texas. In Florida, isolates were collected from six different locations within a 13-km radius near Belle Glade. Three isolates were collected each from Rp1-D and non-Rp sweet corn hybrids. Isolates also were collected from two Rp1-D sweet corn hybrids and a non-Rp sweet corn hybrid near Hondo, TX. Inocula of isolates were increased through one uredinial generation in the greenhouse. Several 1-cm2 pieces of leaf tissue with sporulating uredinia were placed in 15 ml of a solution of water and Tween 20. This inoculum was placed in whorls of five two-leaved seedlings of a susceptible hybrid, 'Primetime.' Urediniospores from newly formed uredinia were collected 10 days later and used as inocula to assay each isolate. Two isolates from Florida (one each from an Rp1-D and a non-Rp hybrid) were assayed on a non-Rp susceptible check, 20 different single Rp genes, and nine compound Rp genes. Other isolates were assayed on two replicates of a non-Rp susceptible check, a source of Rp1-D, and five single Rp genes that were effective against the isolates collected from the Midwest in 1999 and from Mexico in 2000. Each experimental unit consisted of five plants grown in 10-cm-diameter pots. Plants at the two-leaf stage were inoculated three times within 5 days by filling whorls with a urediniospore suspension. Rust reactions were rated 10 days after the final inoculation. Isolates collected in Florida from non-Rp hybrids were avirulent on Rp1-D but those collected in Texas from non-Rp hybrids were virulent on Rp1-D. Isolates collected in Florida and Texas from Rp1-D hybrids had a similar pattern of virulence as isolates collected from the Midwest in 1999 and from Mexico in March 2000; that is, effective single Rp genes included Rp1-E, Rp-G, Rp1-I, and Rp1-K. A source that we previously believed was Rp1-L now appears to be Rp-G. These are the first reports from Florida and Texas of P. sorghi virulent on Rp1-D, and they are the first occurrences of virulence against Rp1-D in the continental U.S. in 2000. Apparently, P. sorghi with virulence against Rp1-D has become established in an area where common rust inocula for North America overwinters. References: (1) J. K. Pataky and W. F. Tracy. Plant Dis. 83:1177, 1999. (2) J. K. Pataky et al. Plant Dis. 84:810, 2000.

Exogenous NO(3) Influx and Endogenous NO(3) Efflux by Two Maize (Zea mays L.) Inbreds during Nitrogen Deprivation.

The influence of nitrogen stress on net nitrate uptake resulting from concomitant (15)NO(3) (-) influx and (14)NO(3) (-) efflux was examined in two 12-day-old inbred lines of maize. Plants grown on (14)NO(3) (-) were deprived of nitrogen for up to 72 hours prior to the 12th day and then exposed for 0.5 hour to 0.15 millimolar nitrate containing 98.7 atom% (15)N. The nitrate concentration of the roots declined from approximately 100 to 5 micromolar per gram fresh weight during deprivation, and (14)NO(3) (-) efflux was linearly related to root nitrate concentration. Influx of (15)NO(3) (-) was suppressed in nitrogen-replete plants and increased with nitrogen deprivation up to 24 hours, indicating a dissipation of factors suppressing influx. Longer periods of nitrogen-deprivation resulted in a decline in (15)NO(3) (-) influx from its maximal rate. The two inbreds differed significantly in the onset and extent of this decline, although their patterns during initial release from influx suppression were similar. Except for plants of high endogenous nitrogen status, net nitrate uptake was largely attributable to influx, and genetic variation in the regulation of this process is implied.